Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3025 PSYC > final exam > Flashcards

final exam Flashcards

1
Q

What does the ‘Hierarchical Taxonomy of Psychopathology’ (HiTOP) depict?

A

It is a framework for understanding the dimensional aspects of symptoms, along with the underlying biological and environmental influences on, different kinds of psychiatric disorders.
Allows for mental health conditions to be represented in terms of severity, intensity and comorbidity rather than the categorical boundaries within the DSM-V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the main components of Spence and Rapee’s model of social anxiety disorder?

A

Performing avoidance/safety behaviours provides relief that reinforces the social anxiety.
Heightened physiological arousal from anxiety can also reinforce that a social situation is threatening/dangerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the biological “fear response” factors that have been shown to be associated with social anxiety disorder?

A

Neurotransmitters: serotonin, norepinephrine, dopamine
Neuroanatomy:
- increased fear circuit amygdala activation
- reduced hippocampal volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the environmental factors implicated in the development of social anxiety disorder?

A
  1. Parenting style -> parent-child attachment
  2. Parent modelling and direct conditioning of behaviours
  3. Peer experiences (rejection, teasing, bullying)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the evaluative processes that occur before a social situation in an individual with social anxiety disorder?

A
  • Anticipatory processing
  • Avoidance behaviours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the evaluative processes that can occur during a social situation in an individual with social anxiety disorder?

A
  • Self-focus
  • Safety or escape behaviour
  • Cognitive avoidance
  • Attentional bias to threat
  • Performance deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the biological factors for generalised anxiety disorder?

A
  • Functional deficiency of GABA neurotransmission
  • Reduced volume in the hippocampus, anterior cingulate cortex and amygdala
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two levels of worry in Well’s ‘meta-cognitive model’ of generalised anxiety disorder?

A
  1. Everyday events -> worry is excessive and out of proportion
  2. Worry about worry (meta-beliefs)
    Plus: unhelpful behaviour such as avoidance or reassurance seeking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the intolerance of uncertainty model?

A

When considering anxiety inducing situations, individuals with generalised anxiety disorder tend to focus on the ambiguous or uncertain aspects of that situation.
People with GAD have a low tolerance for ambiguous situations, which can increase anxiety and discomfort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What issues in the DSM-V does the HiTOP model address?

A
  • Arbitrary boundaries between psychopathology and normality
  • Unclear boundaries between disorders
  • Frequent co-occurrence and heterogeneity of disorders
  • Diagnostic instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the interplay between stress, fear and anxiety

A

Fear and anxiety are usually adaptive processes which involve sympathetic nervous system activity (arousal). Anxiety helps to notice and plan for future threats, whereas fear is fundamental for fight-or-flight reactions.
When the body’s fear response is activated in situations where there is no real danger, it can lead to excessive and chronic levels of stress. The more anxious a person becomes, the more sensitive their body becomes to stress and fear, and the more easily triggered their anxiety becomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What behaviours/processes does intolerance of uncertainty interact with?

A
  • Positive beliefs about worry: rationalisation of worry
  • Poor problem orientation and low confidence
  • Negative reinforcement through avoidance behaviours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the meta-cognitive model of worry suggest about anxiety?

A

The symptomology of anxiety disorders is influenced by negative appraisals of worry (meta-cognitions). Type 1 worry does not constitute a pathology, whereas negative beliefs about worry is what maintains anxiety.
Meta-worry causes an escalation in anxiety and interferes with the use of effective forms of mental control.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the cross-national trends for anxiety disorders?

A

In 2000-2021, approximately 16.8% (3.3 million people) had a 12-
month Anxiety disorder in Australia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the factors of this symptom in the DSM-V:
1. Depressed or irritable mood

A
  • Constant negative affective state, tearfulness, irritability, pessimism
  • Present for the majority of the day, nearly every day, for at least 2 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the factors of this symptom in the DSM-V:
2. Anhedonia

A
  • Impaired ability to experience either pleasure or interest
  • Loss of interest in anything found to be enjoyable in a pre-depressive state
  • Reduced motivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the factors of this symptom in the DSM-V:
3. Appetite/weight disturbances

A
  • Hypophagia: stress decreases desire to eat, often resulting in weight loss
  • Hyperphagia: stress increases desire to eat, often resulting in weight gain
  • Daily fluctuations in appetite, or unintentional change of 5% in body weight within 1 month of other symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the factors of this symptom in the DSM-V:
4. Sleep disturbances

A

Exacerbates other symptoms: memory, mood, concentration
- Insomnia: chronic inability to sleep (initial, terminal or middle forms); 85% prevalence
- Hypersomnia: daily excess of 10hrs of sleep (not restful, increased daytime sleep); 48% prevalence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the factors of this symptom in the DSM-V:
6. Fatigue

A
  • Lethargy linked to mental or physical exertion
  • 2nd most reported symptom (73-97%)
  • Exacerbates other symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the factors of this symptom in the DSM-V:
5. Psychomotor disturbances

A
  • Agitation: feelings or behaviours of restlessness (can’t sit still, talkative, distracted, racing thoughts, mood switches)
  • Slowing: slow thoughts/behaviour (poor eye contact, fixed gaze, poor posture, flat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the factors of this symptom in the DSM-V:
7. Feelings of guilt or worthlessness

A
  • Guilt: feeling bad about uncontrollable circumstances, placing blame on self
  • Worthlessness: inadequacy, low self-esteem, self-loathing; affects 80-85%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the factors of this symptom in the DSM-V:
8. Concentration or memory impairments

A
  • Impaired executive functioning
  • Lowered cognitive inhibition
  • Reduced capacity to problem solve
  • Reduced mental flexibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the factors of this symptom in the DSM-V:
9. Suicidal Ideation

A
  • Passive: thoughts without intent
  • Active: thoughts with intent to act
  • SLAP Assessment: specificity, lethality, availability, proximity
  • 78-89% consider, attempt, contemplate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the kindling effect in MDD?

A

Repeated exposure to stressors + neurochemical changes = more frequent depressive episode without clear cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the global and national prevalence estimates of MDD?

A

Global: 322 million people = 4.5% population; 5.5% males, 3.6% females
Australia: 12-month prevalence 10.4%; 11.6% females, 9.1% males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the heterogeneity in MDD symptom profiles

A

227 potential presentations that qualify for diagnosis, caused by interaction between pathogenesis and aetiological factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are main assessment tools for MDD in adults?

A

Clinician administered:
Mini International Neuropsychiatric Interview (MINI)
Hamilton Depression Rating Scale (HAM-D)
Montgomery-Asberg Depression Rating Scale (MADRS)
Self-report:
Beck Depression Inventory (BDI-II)
Depression, Anxiety, and Stress Scale (DASS)
Centre for Epidemiological Studies Depression Scale (CES-D)
Patient Health Questionnaire (PHQ-9)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the main assessment tools for MDD in both children and older adults?

A

Children:
Child Behaviour Checklist (CBCL)
Children’s Depression Rating Scale (CDRS)
Older Adults:
Geriatric Depression Rating Scale (GDRS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe Beck’s cognitive model of depression

A

Stressful life events in early life shape schemas.
Negative cognitive schemas are triggered by negative interactions, repeated activation leads to an attentional bias towards negative stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the learned helplessness model of MDD

A

When a person believes that they have no control over their circumstances they will begin to behave as if they are helpless, which is a learned behaviour/belief.
Universal: nothing can be done about the situation -> external attributions
Personal: other’s could fix the situation, but not the individual -> internal attributions
Both universal and personal types cause depressive symptoms as the individual learns/believes to not expect change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the monoamine hypothesis of depression?

A

Low levels of serotonin, norepinephrine and dopamine in the brain are related to depressive symptoms:
- Norepinephrine: energy, alertness, concentration
- Dopamine: reward, anhedonia
- Serotonin: mood, appetite, anxiety, suicidal ideation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is the HPA axis hypothesised to be related to depression?

A

Hypothalamic Pituitary Adrenal axis is responsible for feedback loops between the brain and pituitary/adrenal glands which are involved in the stress response (and others) by modulating the release of cortisol and other neuroendocrinic factors.
Hyperactivity of the HPA axis has been shown to relate to depressive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does the prefrontal cortex do ?

A

Regulates executive function -> broader changes in activation patterns is thought to be due to repeated exposure to stress hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does increased activity in the ventromedial prefrontal cortex predict?

A

Negative emotions, such as low mood and fear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does increased activity in the orbitofrontal prefrontal cortex predict?

A

Decreased emotional regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does increased activity in the dorsolateral prefrontal cortex predict?

A

Deficits in memory, attention and reasoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is one hypothesised neuroanatomical cause for anhedonia?

A

Reduced volume in the anterior cingulate cortex, leading to hypoactivation which manifests as blunted affect, anhedonia and reduced coping abilities

37
Q

How is the hippocampus implicated in MDD?

A
  • Greater activation for negative stimuli -> negative biases and formulation of negatively valanced cognitions
  • Smaller hippocampal volumes -> leads to earlier onset and more episodes
  • Linked to memory impairment and cognitive decline
38
Q

How is the amygdala implicated in MDD?

A
  • Greater activation for negative stimuli, which remains elevated, suggesting that the amygdala is implicated in long-term changes to emotional processing
  • Hyperactivation of blood-flow and glucose metabolism mechanisms which manifests as a bias toward emotional stimuli, increased low mood
39
Q

What is the interpersonal theory of depression?

A

Depressive symptoms + excessive reassurance seeking = interpersonal difficulties
Rejection from others increases reassurance seeking.
Individual with MDD interprets frustration with reassurance seeking as rejection.

40
Q

What are the four main classes of antidepressants?

A

Selective Serotonin Reuptake Inhibitors (SSRIs)
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
Tricyclic Antidepressants (TCAs)
Monoamine Oxidase Inhibitors (MAOIs)

41
Q

What are the comparative efficacies of the classes of antidepressants?

A

SSRIs and SNRIs > placebo
SSRIs > SNRIs, but greater side effects
MAOIs > TCAs, less adverse effects

42
Q

What are the goals of CBT for depression?

A

Reduce the frequency and severity of negative thoughts; improve cognitive and emotional functioning
Cognitive restructuring: teaching rationalisation of negative thoughts and supplementation with more realistic or positive ones

43
Q

What are the four DP framework principles?

A
  1. Atypical development
  2. Equifinality and multifinality
  3. Risk and protective factors
  4. Adaption and resilience
44
Q

Describe this developmental psychopathology principle:
1. Atypical development

A

Conceptualisations of typical development provides a crucial comparison for understanding what is considered atypical development.
Culture and social factors shape the development of psychology.

45
Q

Describe this developmental psychopathology principle:
2. Equifinality and multifinality

A

Equifinality: similar risk factors may develop different outcomes
Multifinality: different risk factors may develop the same disorder
There are no definitive pathways to psychopathology

46
Q

Describe this developmental psychopathology principle:
3. Risk and protective factors

A

Risk factors: genetic predispostions, adverse childhood experiences, SES, environmental stressors
Protective factors: support network, resilience, coping skills

47
Q

Describe this developmental psychopathology principle:
4. Adaption and resilience

A

Factors that promote adaption and resilience in the face of adversity to explain why some individuals thrive following risk exposure

48
Q

How does the Developmental Psychopathology (DP) Framework differ from the DSM-V in conceptualisations of child psychopathology?

A

Biological, psychological and environmental factors contribute to shaping development over the lifespan. DP Framework considers development as a continuous process rather than distinct or abrupt stages

49
Q

What is the percentage breakdown of the trajectory child/adolescent antisocial (externalising) psychopathology?

A

Not antisocial: 70%
Childhood limited (5-7 years): 7%
Adolescent onset (wanes into adulthood): 15%
Early onset persistent (consistently antisocial behaviour across the lifespan): 8%

50
Q

What are externalising disorders characterised by?

A

Under-controlled or inability to control behaviour

51
Q

What are the personal risk and maintaining factors for ODD and CD?

A

Temperament: high/low emotional reactivity, low effortful control, CU
Neuropsychological: low IQ, learning difficulties
Cognitive: dysfunctional social cognition, low self-esteem
Emotional: dysregulated affect, emotion recognition biases/deficits

52
Q

What are the family risk and maintaining factors for ODD and CD?

A

Parenting: harsh/inconsistent, low warmth parenting, insecure attachment, poor communication, low monitoring
Family stressors: trauma, abuse, parental incarceration, parental psychopathology

53
Q

What are the social risk and maintaining factors for ODD and CD?

A

School: problematic teacher relationship, bullying
Peers: rejection, affiliation with deviant peers, risky sexual behaviour
Community: exposure to community violence, poverty, discrimination

54
Q

What are callous-unemotional (CU) behaviours?

A

Individual has a callous lack of empathy and evident lack of remorse; deficient affect and lack of concern about performance or others

55
Q

Describe the parent-child coercive cycle

A

Child’s non-compliance leads to intensified direction from parent.
If comply: negatively reinforces parent’s angry/intimidating behaviour
If parent gives up: negatively reinforces child’s behaviour

56
Q

What is the heritability estimate for ADHD?

A

70-80%

57
Q

Which brain areas have been found to be smaller in children with ADHD?

A

Amygdala, hippocampus

58
Q

When is a child diagnosed with ODD?

A

When they do not meet the criteria for conduct disorder, but still exhibit behaviour such as losing their temper, arguing with adults, refusing to comply, deliberately annoying others, being angry, touchy or vindictive.

59
Q

Describe parent management training for conduct disorder

A

Parents are taught to modify their responses to their children so that prosocial rather than antisocial behaviour is consistently rewarded

60
Q

What are the symptoms for depression in children aged 7-17?

A
  • Depressed mood
  • Inability to experience pleasure (anhedonia)
  • Fatigue
  • Concentration issues
  • Suicidal ideation
61
Q

What are treatment options for childhood anxiety?

A

Coping Cat CBT: focused on confrontation of fears, development of new ways to think about fears, exposure and relapse prevention
SPACE: focused entirely on parents, involving psychoeducation, but also efforts to teach parents how to bolster coping skills and confidence in children

62
Q

Define echolalia

A

A symptom of autism where the child echoes, usually with remarkable accuracy, what they have heard another person say, either immediately or delayed

63
Q

What are the heritability estimates of ASD?

A

Between 60-90%

64
Q

What are the neurological factors behind ASD?

A

Brains of adults and children with ASD are larger, grow between ages 1-4. Brain overgrowth may mean that neurons are not being pruned correctly, which is important for brain maturation.
Areas of the brain that are overgrown include frontal, temporal and cerebellar regions which are linked to language, social and emotional functions

65
Q

What are the positive symptoms of psychosis?

A
  • Hallucinations
  • Delusions
  • Disordered thought
  • Disordered/abnormal motor behaviour
66
Q

What are the negative symptoms of psychosis?

A
  • Affective flattening
  • Anhedonia
  • Alogia (speech poverty)
  • Avolition (loss of drive)
  • Social withdrawal
67
Q

Define hallucinations

A

Perception-like experiences with the clarity of true perception but without the external stimulation of the relevant sensory organ

68
Q

What are the covered theories of hallucination?

A

Dysfunctional metacognition: unable to identify the context of thoughts/emotions to integrate into larger representations
Dysfunction in perception: altered activity in speech production/processing brain regions suggesting that there might be alterations in auditory processing pathways
Misattribution: internal cognitive events being misattributed to an external source, dysfunction in motor system predicted and actual states

69
Q

Define delusions

A

False belief based on incorrect inference about external reality that is firmly held despite evidence to the contrary

70
Q

What are the five phases of schizophrenia?

A
  1. Premorbid: risk factors
  2. Prodromal: further deterioration of functioning (mood symptoms, issues socially, brief psychosis symptoms)
  3. Acute: symptoms manifest in entirety
  4. Early recovery: improvement, can be accompanied by depressive or anxious symptoms
  5. Late recovery: ideally reintegration into social life, high likelihood of relapse
71
Q

What are the symptoms of schizoid personality disorder?

A
  • Introversion
  • Voluntary withdrawal from social interactions
72
Q

What are the symptoms of schizotypal personality disorder?

A
  • Magical thinking
  • Odd behaviour
    + Schizoid symptoms
73
Q

What are the symptoms of Schizophrenia?

A

Psychosis + schizotypal symptoms

74
Q

What are the symptoms of Schizo-affective disorder?

A

Schizophrenic symptoms + mood disorder

75
Q

What are the durations of the relevant schizophrenic disorders?

A

Brief psychotic disorder: 1 day - 1 month
Schizophreniform disorder: 1-6 months
Schizophrenia: 6 + months

76
Q

What is the heritability estimate of schizophrenia?

A

81% -> 9% for first degree relatives -> 27% for children of two affected parents

77
Q

Which brain areas are have reduced volume in individuals with schizophrenia?

A

hippocampus, amygdala, thalamus, nucleus accumbens, intercranial space

78
Q

What is the dopamine hypothesis of schizophrenia?

A

People with schizophrenia are tend to have higher concentration and greater activity of dopaminergic neurons. Chlorpromazine, which is a dopamine receptor antagonist, is used as a pharmacological treatment for schizophrenia to address psychotic symptoms

79
Q

Describe the diathesis-stress model

A

The likelihood of developing a disorder or a disorder’s trajectory is a result of an interaction between predispositional vulnerability and exposure to stressors. If an individual’d tolerance to stressors is overwhelmed -> presentation of symptoms

80
Q

What are the statistics of cannabis use’s effects on schizophrenia?

A

Individuals who use cannabis are 3.9 times more likely to be at risk for psychosis compared to individuals who do not

81
Q

What is the severity breakdown of substance use disorder?

A

Mild: 2-3 symptoms
Moderate: 4-5 symptoms
Severe: 6+

82
Q

What are the stages in the process model of addiction?

A
  1. positive attitude
  2. experimentation
  3. regular use
  4. heavy use
  5. dependence or abuse
83
Q

What is the comorbidity of substance use disorder?

A

37% of those with alcohol use disorder and 53% with drug use disorder have a comorbid mental illness

84
Q

What does the half-life of a drug mean?

A

Time for half the drug to be removed from the body -> tied to drug abuse and withdrawal. The shorter a drug’s half-life, the stronger its addictive properties

85
Q

Describe reward deficiency syndrome

A

Underactive reward circuitry within the brain that increases susceptibility to the rewarding effects of drugs/ addictive behaviours

86
Q

Which pathway in the brain is important for stimulus-reward processing?

A

Mesolimbic pathway

87
Q

Which pathway in the brain is important cognitive control, and motivation and emotion processing?

A

Mesocortical pathway

88
Q

What are the 6 stages in the Behaviour Change Theory model for addiction?

A
  1. Pre-contemplation: no intention to start change/unaware of need
  2. Contemplation: intention to start change/ambivalence
  3. Preparation: ready to start/concern of failure
  4. Action
  5. Maintenance
  6. Relapse
89
Q

What are the biological treatments for substance addiction?

A
  • Detoxification
  • Replacements (reduce withdrawal)
  • Antagonists (block rewards)
90
Q

What are the psychological treatments for substance addiction?

A
  • Aversion therapy: paired negative stimulus with drug
  • 12-step programs
  • CBT: stimulus control and contingency management, coping, connection with values
  • Motivational interviewing

3025 PSYC (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions